326 Abnormal Psychology
psychosis. For some years he conducted research on the
effects of various febrile illnesses (e.g., tuberculosis) on
patients with diagnosis of psychosis, reporting some suc-
cesses and many failures. In 1917 he treated some general
paresis patients with blood from a patient infected with
malaria. Three of them died, and not until 1919 was he able
to define the kind of malarial infection that would be benefi-
cial. Others quickly accepted his technique, and in 1924 he
received the Nobel Prize for this discovery.
The exact manner in which these effects occurred was a
matter of speculation, many physicians concluding that the
high heat of the fever itself killed the organisms causing the
syphilitic infection. Other methods of generating high heat
were employed, including hot baths, hot air, radiothermy,
electric blankets, and so forth. The general success of the
fever treatment prompted an attempt to apply it to cases of
schizophrenia, manic-depressive psychosis, and other psy-
chiatric syndromes. These were unsuccessful, and the use of
malarial fever treatment in GPI was abandoned with the dis-
covery of penicillin (Shorter, 1997).
Comas and Convulsions
The first extensive systematic use of treatments intended to
induce convulsions and/or coma was reported by Manfred
Sakel (1900–1957). While treating drug addicts in a Berlin
sanitarium, Sakel accidentally gave an overdose of insulin to
one patient who also had diabetes. The patient became
comatose, but on recovery appeared to have lost her craving
for drugs. Sakel began to apply insulin as a treatment for
addiction. A later accidental overdose was given to a patient
who was also psychotic. In this case, the patient’s psychosis
appeared to be much reduced, inspiring Sakel to develop
insulin coma treatment for schizophrenia. He reported that
he had observed many successful outcomes but, as usual, no
independent objective evaluation of the improvement was
conducted (Sakel, 1935). This procedure became widespread
until it was displaced by the use of the synthetic chemical
metrazol.
In 1935, a Hungarian physician J. L. Von Meduna
(1896–1964) reported that he had discerned subtle differ-
ences in the brain cells of epilepsy and schizophrenia
patients. He inferred that epilepsy and schizophrenia were
antagonistic and that schizophrenia might be treated by in-
ducing convulsions. On the basis of experiments with ani-
mals, Meduna (1935) decided to use camphor injections but
soon switched to metrazol and reported impressive improve-
ments in his patients. By the 1940s, metrazol shock (convul-
sion) therapy was widespread in the psychiatric hospitals of
the United States. Some evidence indicated that metrazol was
effective with depressed patients, but not with schizophrenia
patients, and it was ultimately replaced with electroconvul-
sive treatment (ECT). In the case of both insulin coma and
metrazol-shock the basic initial observations had been acci-
dental; no accepted theory existed regarding the biological
mechanisms that might account for the reported effects and
little appears to have been attempted to develop one.
In 1937 two psychiatrists, Cerletti and Bini (1938), pre-
sented an account of their use of ECT of sufficient strength to
produce convulsions and coma in psychiatric patients, some
of whom showed an improvement in clarity of thinking and
general reality contact. Although the procedure was applied
rather widely to psychotic patients and especially schizophre-
nia patients, the results were discouraging. Huston and
Locher (1948), for example, found no difference in the rate of
improvement in depressed patients treated with ECT com-
pared with untreated patients. In addition, improvement in
the untreated lasted longer than in the treated patients. Later
studies of damage attributable to ECT (Alpers & Hughes,
1942) showed destructive effects to brain tissue. Again, no
satisfactory theory accounted for the effects of the treatment.
Gordon (1948) listed no fewer than 50 hypotheses, ranging
from the belief that the patient had experienced the convul-
sion as death and rebirth, to the view that the shock acted as a
stressor and stimulated stress-resistance mechanisms in bod-
ily functioning (Maher, 1966, pp. 499–500). Today, ECT is
used sparingly and then mainly with certain kinds of affective
disorder.Experimental PsychopathologyExperimental investigation of psychopathology was stimu-
lated by the methods that were being developed to measure
the psychological processes of healthy individuals in labora-
tories of experimental psychology in the latter part of the
nineteenth century. Although its beginnings were modest,
experimental investigations of psychopathology were to
expand throughout subsequent decades.KraepelinInvestigation of psychopathology using the methods of scien-
tific experimental psychology began with the work of Emil
Kraepelin (1856–1926), who established a laboratory in
Heidelberg in 1890, where he conducted experimental stud-
ies of psychiatric patients. His work attracted others to join
his laboratory, notably British psychologist/anthropologist
William Rivers, and American psychiatrist, August Hoch.
Rivers (1895) and Hoch (1904) published translations of some
of the work done at Heidelberg, but much of Kraepelin’s